Acyclovir mechanism of action operates via a sophisticated mechanism to combat viral infections caused by herpes simplex virus (HSV) types 1 and 2, as well as varicella-zoster virus (VZV). Upon entering the body, acyclovir undergoes a series of transformations orchestrated by viral thymidine kinase, an enzyme unique to infected cells. This process converts acyclovir into its active form, acyclovir triphosphate, within the infected cell.
Acyclovir mechanism of action triphosphate operates as a nucleoside analogue, mimicking the structure of guanosine triphosphate, a crucial building block for viral DNA replication. When the virus attempts to replicate its DNA, it mistakenly incorporates acyclovir triphosphate instead of guanosine triphosphate into the viral DNA chain, effectively halting DNA synthesis. Consequently, the viral DNA chain becomes incomplete and non-functional, rendering the virus unable to replicate and spread within the body.
By disrupting viral DNA synthesis, acyclovir impedes the replication and proliferation of herpes viruses, ultimately curbing the progression of infections. This mechanism of action specifically targets infected cells, minimizing adverse effects on healthy cells. Acyclovir’s precise interference with viral replication makes it a cornerstone in the treatment of herpes infections, offering relief from symptoms and accelerating the healing process. Understanding the intricacies of acyclovir’s mechanism of action illuminates its effectiveness in combating viral infections and underscores its importance in clinical practice.
